We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Respiratory Toxicity of Aged Paint Particles on a Building Exterior Wall.
Summary
When exterior building paint ages and flakes off, it breaks down into tiny microplastic particles that can be inhaled. In a study on mice, breathing in these paint particles for several weeks caused lung inflammation and damage, blood changes, and impaired function of immune cells that normally protect the lungs—with female mice showing more severe effects than males. This suggests aged paint dust could be an overlooked source of harmful air pollution, and more research is needed to understand the risks to people who breathe it in over time.
Architectural exterior paints play a crucial role in protecting building materials from aging and corrosion. We obtained pieces that fell from the exterior of a university building and ground them using a miller. Aged paint particles (APPs) contained a high concentration of titanium and showed C-H bonds, indicating the presence of microplastics. APP had negatively charged surfaces and were agglomerated in the vehicles used in this study. When exposed repeatedly to APP via pharyngeal aspiration for 13 weeks, a decrease in platelet count and an increase in total cholesterol level were observed in female mice exposed to APP. The increases in levels of pulmonary inflammatory mediators and the lesion severity following exposure to APP were more remarkable in female mice than in male mice. Extramedullary hematopoiesis was also found in the spleens of female mice but not in male mice exposed to APP. Using MH-S cells derived from murine alveolar macrophages, we also found that cell viability decreased markedly even at the lowest concentration and that nitric oxide production, an intracellular second messenger, increased rapidly at the highest concentration. Meanwhile, ATP production was not notably changed in APP-treated cells. Moreover, the expression of all innate immune-related genes and renin-angiotensin-aldosterone system-related genes was downregulated in APP-treated cells compared to the control, and the expression of unfolded protein response genes was lower in the ER but higher in mitochondria. Taken together, we suggest that dysfunction of alveolar macrophages, the primary defenders against inhaled foreign materials, may underlie APP-induced pathological changes. Additionally, we believe that, as a significant source of microplastics and a potential disease-causing ambient pollutant, APP should be removed from the environment under strict control. Considering the biological responses observed in subchronic exposure, we also propose that further study is needed to clarify the health effects of chronic respiratory exposure to different types of APP.